Coronary Artery Disease in Masters-Level Athletes

Preparticipation screening 

Screening masters-level athletes before training and sports participation is essential to identify preexisting CAD and to reduce risk of coronary events.6 In athletes diagnosed with CAD, screening helps determine if athletic performance can be resumed. Screening commences with a history and physical examination (appendix 1).7

A 12-lead electrocardiogram and echocardiography can identify previous MI and other CVDs, including HCM and arrhythmias. A symptom-limited exercise stress test is vital in screening masters-level athletes. Ideally, it should approximate the cardiovascular, metabolic, and mechanical demands of the intended training and sport. An ST-segment depression greater than 1mm denotes ischemia. Athletic risk is associated with the degree of ST depression, hypotensive blood pressure response, ventricular arrhythmias, and reduced exercise capacity. Failure to achieve age-predicted heart rate on the exercise stress test correlates with future cardiac events.8 Cardiac imaging with echocardiography or nuclear perfusion increases sensitivity and specificity of the exercise stress test.

The exercise stress test should be performed with the athlete continuing medications that will be taken during training and competition. Of note, some cardiac medications (eg, β-blockers) are banned substances in selected sports.

Screening for CAD in a disabled athlete, such as a wheelchair athlete or paralympian, requires special consideration. Exercise stress testing with an upper-body ergometer or hand bike may not achieve target heart rates (85% of age- and sex-predicted maximum heart rate) sufficient to maximize the sensitivity and specificity needed to assess for CAD. Pharmacologic myocardial stimulation to the required heart rate is essential, and nuclear imaging is recommended for greatest yield. However, a pharmacologic stress test is not a functional test and does not mimic the physiologic stress of sports participation.

Special consideration is also needed when interpreting exercise-induced electrocardiographic changes in women. Accuracy may be limited by a higher prevalence of resting electrocardiographic changes, a lower prevalence of severe CAD, hormonal factors (endogenous or replacement estrogens) and the inability of many women to exercise to maximum aerobic capacity during stress testing.9, 10

The exercise electrocardiogram’s sensitivity and specificity for detecting CAD in asymptomatic people are lower for women (61% and 70%, respectively) than men (72% and 77%, respectively).11 This difference may result in false-positive exercise stress test results that lead to further unnecessary and more invasive testing or to limitation of or exclusion from sports participation. Adjunctive data from the exercise stress test improves diagnostic accuracy in women. Enhanced heart rate recovery by 1 or 2 minutes after cessation of the test and a greater functional capacity shown on the test have substantial prognostic value. Women with an abnormal resting electrocardiograph or those believed to be at risk for CAD should be considered for echocardiographic or nuclear imaging during the exercise stress test.10

A greater than 50% narrowing of the luminal diameter detected during coronary angiography is significant. In the absence of significant luminal narrowing, intravascular ultrasound (IVUS) identifies subendothelial atherosclerotic plaques at risk of rupture. Measures of coronary calcification by computed tomography correlate with atherosclerosis and risk of coronary events.12 Other screening tools include cardiac magnetic resonance imaging, ambulatory Holter electrocardiography, tilt table, and electrophysiologic stimulation.

Sports classifications 

Sports are classified according to the predictable cardiovascular responses and bodily impact expected. All sports are classified as dynamic or static—or a combination of both—as shown in table 1.

Table 1. Cardiovascular Responses to Dynamic and Static Exercise

	Response	Dynamic	Static
	Relative force generation	Small	Large
	Joint movement	Large	Minimal
	Change in muscle length	Rhythmic	Minimal
	Predominant metabolic pathway	Aerobic	Anaerobic
	Increases in O2 consumption, cardiac output, SV	Marked	Small
	Systolic blood pressure	Increased	Increased
	Diastolic blood pressure	Decreased	Increased
	Left ventricular load	Volume	Pressure
	Changes after training
	V̇o2max	Markedly increased	No to minimal increase
	a-vo2	Markedly increased	No to minimal increase
	Skeletal muscle enzymatic changes	Increased oxidative enzymes	Increased glycolytic enzymes
	Skeletal muscle mass	No change	Increased
	Ventricular hypertrophy	Eccentric hypertrophy	Concentric hypertrophy

Abbreviations: a-vo2, arteriovenous oxygen difference; SV, stroke volume; V̇o2max, maximum oxygen consumption.

The intensity of dynamic and static exercises ranges from low to high. Myocardial oxygen (MVO2) requirement, which is predominantly influenced by heart rate and systolic blood pressure responses, depends on both the intensity and the type of exercise. When MVO2 is exceeded, ischemia develops. Figure 1 presents a matrix in which sports are classified according to peak static and dynamic intensity achieved during competition.13 Although developed for younger athletes, extrapolation of this classification for the masters-level athlete is acceptable. Other factors that influence cardiovascular responses to exercise include electrolyte abnormalities, emotional stress, altitude, humidity, temperature, and training regimens.

View Large Image Download to PowerPoint

Fig 1. Sports classification matrix, from static to dynamic levels. The increasing dynamic component is defined in terms of the estimated percentage of maximal oxygen consumption (V̇o2max) achieved and results in an increasing cardiac output. The increasing static component is related to the estimated percentage of maximal voluntary contraction (MVC) reached and results in an increasing blood pressure load. The lowest total cardiovascular demands (cardiac output and blood pressure) are shown in green and the highest in red. Blue, yellow, and orange depict low moderate, moderate, and high moderate total cardiovascular demands. NOTE: Higher intensities (V̇o2max/MVC) may be reached during training. *Danger of bodily collision. †Increased risk if syncope occurs. Source: Mitchell et al.13 Reprinted with permission.

Athletes with CAD are placed in 1 of 2 risk categories (table 2). They are considered at substantial risk if any of the risk factors noted are present. For athletes considered at mildly increased risk, low-intensity dynamic (class 1A) and low- to moderate-intensity static (classes 1A and 2A) sports are recommended (see fig 1).14 Masters-level athletes with an overall clinical profile suggesting a very low exercise risk may be allowed to exercise at higher intensity levels. A cautious approach must be taken, with new symptoms prompting a clinical reevaluation and review of the risk categorization. Athletes must be counseled regarding possible symptoms and signs and must be educated about the risk of cardiac events. Athletes stratified as having substantially increased risk are restricted to low-intensity dynamic and static sports (class 1A).

Table 2. Risk Categorization of Athletes with CAD

	Risk Area	Mild Risk	Substantial Risk
	Left ventricular systolic function	Normal. EF >50%	Reduced. EF <50%
	Exercise tolerance for age⁎	Normal	Reduced
	<50y >10 METS
	50–59y >9 METS
	60–69y >8 METS
	>70y >7 METS
	Exercise-induced ischemia	Absent	Present
	Significant coronary stenosis	Absent	Present
	Myocardial revascularization	Successful	Incomplete

Abbreviations: EF, ejection fraction; METS, metabolic equivalents.

⁎ One MET unit implies the consumption of 3.5mL of o2·kg−1·min−1.

After a recent cardiac event, inpatient and/or outpatient cardiac rehabilitation is recommended. Progression to athletic performance after outpatient cardiac rehabilitation is guided by a postrehabilitation exercise stress test and response to increasing training intensities under monitored settings.

Myocardial ischemia can be caused by coronary vasospasm without atherosclerosis. Low-intensity sports (class 1A) are recommended. Myocardial bridging, in which a coronary vessel tunnels within the myocardium, can also lead to exercise-induced ischemia. However, without evidence of inducible ischemia, all competitive sports are allowed according to documented exercise capacity. With ischemia or history of infarction, only class 1A sports are permissible. After surgical correction of the myocardial bridge, if the exercise stress test results are negative, all sports are allowed. After cardiac transplantation, accelerated coronary atherosclerosis is noted in the donor heart. Cardiac evaluation is complex because of altered physiologic parameters at rest and in response to exercise. The IVUS improves the sensitivity of screening for atherosclerosis. Athletes with no abnormalities detected can participate in all sports. With atherosclerosis, evaluation and stratification is as for those with CAD.

Masters-level athletes should be rescreened annually with noninvasive testing that includes history, physical examination, electrocardiogram, echocardiogram, and exercise stress test. Risk stratification and athletic participation are revised accordingly. New symptoms, signs, or unexpected decline in performance warrant immediate cessation of sports and thorough reevaluation. Education of the athlete regarding risks of sports participation must be emphasized. Legal issues regarding physician recommendations of athletic participation have recently been documented.15